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NSx Neuroanatomy > Visual System > Flashcards

Visual System Flashcards

1
Q

Posterior INO of Lutz

A
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2
Q

Categories of eye movement?

A

Conjugate

Vergence

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3
Q

Types of conjugate eye movement

A

Horizontal:

Saccadic

Smooth pursuit

Vestibulo-ocular reflexes

Vertical:

Vertical

Smooth pursuit

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4
Q

What is the purpose of conjugate eye movements?

A

To keep fovea of both eyes fixed on target object (fovea is at the centre of the macula) to maintain binocular vision

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5
Q

What are vergence eye movements?

A

Axis of eyes do not move in parallel

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6
Q

At what distance do vergence eye movements end?

A

>30m, beyond this the axes of the eyes are no longer parallel.

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7
Q

What is common final pathway for conjugate horizontal eye movements

A

CN6 (interneuron) -> contralateral MLF -> CN3 (MR portion)

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8
Q

Which nuclei are connected by MLF

A

3, 4, 6, 8, 11

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9
Q

What is the cortical centre for horizontal saccadic eye movement?

A

Contralateral FEF (Frontal lobe)

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10
Q

What is the pontine centre for saccadic eye movements

A

Ipsilateral PPRF

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11
Q

Describe cortical generation of left saccadic horizontal conjugate gaze

A

Right FEF-> Descending fibres-> Left PPRF -> Abducens (motor)-> LR

+

Abducens (interneuron)- > right MLF to right CN3-> Right MR

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12
Q

Where is the FEF found

A

Posterior middle frontal gyrus (in front of precentral gyrus)

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13
Q

How do descending fibres from the FEF reach the PPRF

A

Either directly or via the ipsilateral superior colliculus

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14
Q

Conjugate gaze palsy in FEF destruction

A

Towards affected size

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15
Q

Conjugate gaze palsy in FEF activation (e.g. seizure)

A

Away from affected side

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16
Q

Conjugate gaze palsy due to PPRF destruction

A

Away from affected side

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17
Q

The manifestation of right MLF lesion?

A

When left eye abducts, the right eye will not adduct.

There is compensatory nystagmus of the left eye

INO

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18
Q

Common causes of unilateral INO

A

Most common:

Demyelinating lesions e.g. MS.

CVA (e.g. brainstem infarction)

Trauma

Fourth ventricular tumours

SLE

Phenothiazine toxicity

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19
Q

The manifestation of bilateral INO

A

Abduction of outer eye is preserved in both eyes but neither eye will adduct.

There will be nystagmus

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20
Q

The most common cause of bilateral INO

A

Young: Inflammatory demyelinating condition

Old: Infarct or haemorrhage

Large tumours

Wernicke’s encephalopathy.

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21
Q

What is the difference between internal, external and INO?

A

External ophthalmoplegia= EOM paralysis but pupil working

Internal opthalmoplegia= pupil not working but EOM working

INO= ophthalmoplegia due to internuclear lesions.

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22
Q

How to differentiate between adduction palsy due to INO and adduction palsy due to damage to CN3 branch to medial rectus?

A

In INO adduction is preserved with convergence as pathways do not require MLF.

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23
Q

Manifestation of left 1 and a half syndrome?

A

Loss of ipsilateral horizontal movement

Loss of contralateral adduction but not abduction

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24
Q

Possible causes of 1 and a half syndrome?

A

Damage to ipsilateral PPRF and MLF

Or

Damage to ipsilateral, CNVI and MLF after it has crossed the midline from its site of origin.

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25
Q

The consequence of bilateral FEF damage?

A

Oculomotor apraxia

Nerves to EOM are intact, defect is in cortical saccadic generators bilaterally.

Preserved smooth tracking and VOR

https://collections.lib.utah.edu/ark:/87278/s64v2kqk

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26
Q

What structure within the semicircular canal detects rotational movements?

A

Collection of hair cells in the ampulla called the cristae. (cupula)

Endolymph moves towards the ampulla causing stimulation of the cupula

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27
Q

What is Scarpa’s ganglion?

A

Afferent ganglion receiving fibres from the hair cells of the cupula of the semicircular canal

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28
Q

What is the main vestibular nucleus involved in VOR?

A

Medial vestibular nucleus

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29
Q

How is the medial vestibular nucleus connected with the contralateral abducens?

A

Via the MLF

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30
Q

With the leftward rotation of the head, what happens to the endolymph in either horizontal semicircular canal?

A

On the left endolymph is ampullopetal (i.e. towards the ampulla)

On the right endolymph is ampullofugal

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31
Q

What is the consequence of ampullofugal flow?

A

Endolymph moves away from kinocilium leading to inhibition

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32
Q

What happens to the VOR in an alert person on rightward rotation?

A

There is a slow conjugate horizontal movement towards the left, then right beat nystagmus due to cortical input - frontal lobe (corrective movement)

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33
Q

Why does warm water cause the eyes to deviate towards the contralateral side in the VOR?

A

Warm water causes expansion of endolymph, causing ampullopetal movement and stimulation of the kineocilia

In the conscious patient the fast phase of nytagmus will be towards the same side (COWS)

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34
Q

What happens when cold water is put into the right ear?

A

Eyes will deviate towards the same side, fast phase of nystagmus will be towards the contralateral side (COWS)

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35
Q

Explain COWS

A

In an alert patient during caloric testing.

Warm water into the right ear will cause eyes to deviate to the left, there will be fast phase nystagmus to the right (Warm same)

Cold water into the right ear will cause eyes to deviate to the right, there will be fast phase nystagmus to the left (Cold opposite)

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36
Q

Give reasons why optic nerve is not a nerve

A

Covered by oligodendrocytes

Affected by MS

Does not regenerate

Originates from diencephalon

Covered by meninges not epineurium

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37
Q

Describe the embryological development of the retina

A

Outpouching from neuroectoderm (optic vesicle)

Invaginated by the lens and becomes a double-layered optic cup

The outer part of the cup makes the choroid

Inner part makes the retina

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38
Q

Etymology of macula lutea?

A

Macula- spot

Lutea- yellow

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39
Q

Difference between macula lutea and fovea centralis?

A

Fovea contains maximal concentration of cones.

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40
Q

What is the differnece in the chemicals found in rods vs cones

A

Rods- Rhodopsin

Cones- iodopsin

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41
Q

Type of vision perceived by rods?

A

Scotopic

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42
Q

Type of vision perceived by cones?

A

Photopic

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43
Q

Which artery supplies the fovea?

A

Supplied by diffusion from the choroid, relatively avascular

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44
Q

What are the layers of the retina?

A

Pigment epithelial cells

Rod/Cone cells

Outer limiting membrane

Outer nuclear layer

Outer plexiform layer

Inner nuclear layer

Inner plexiform layer

Inner ganglion cells

Nerve fibre layer

Inner limiting membrane

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45
Q

From where do the first five (outer) layers of the retina derive their blood supply?

A

Diffusuion from choroid

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46
Q

Ganglion cells synapse where?

A

LGB

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47
Q

What is the most common site of retinal detachment?

A

Between pigmented epithelial layer and rod and cone layer

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48
Q

What is the destination of post-chiasmal fibres

A

Around 90% to ipsilateral LGN

Around 10% to the pretectal nucleus

49
Q

How many layers of cells are there in the LGN?

A

6 layers

50
Q

Into which layer of the LGN do ipsilateral (i.e. temporal retinal) optic tract fibres from the optic tract synapse?

A

2, 3, 5

Contralateral arrive in 1,4, 6

51
Q

Which midbrain structure are involved in visual pathway?

A

Superior colliculus

Pretectal nucleus

CN3 motor nucleus

EW nucleus

52
Q

Where do the 10% of optic tract fibres not reaching the LGN body synapse?

A

In the midbrain:

Superior colliculus

and

Pretectal nucleus

53
Q

What is the name of the tract of fibres from the optic tract to the midbrain?

A

Superior brachium

54
Q

Possible cause of bilateral nasal hemianopia?

A

Bilateral carotid artery masses

Calcification of the internal carotid arteries can impinge the uncrossed, lateral retinal fibers, leading to loss of vision in the nasal field.

55
Q

Left homonoymous hemianopia

RAPD

Location of lesion

A

Optic tract (loss of fibres to pretectal nucleus)

56
Q

Blood supply to the macula region of the occipital cortex?

A

PCA and MCA

57
Q

Visual field deficit

BIlateral cuneal damage

A

Bilateral lower altitudinal hemianopia

58
Q

Visual field defect

Bilateral lingual gyri destruction

A

Bilateral upper altitudinal hemianopia

59
Q

Unilateral altitudinal hemianopia

Lesion location

A

Prechiasmal

60
Q

Location of lesion

Monocoular visual loss with temporal upper quadrantopia

A

Optic nerve immediately adjacent to the chiasm.

61
Q

Outline the pupillary light reflex

A

Light->Retina-> optic nerve-> chiasm-> tract-> superior bravchium)->pretectal nucleus (superior colliculus)-> EW nucleus bilatearlly-> CN3-> Ciliary ganglion-> pupillary constriction

62
Q

What pathway connects both pretectal nuclei?

A

Posterior commissure

63
Q

Which nerve carries postganglionic fibres from the ciliary ganglion?

A

Short ciliary nerve

64
Q

What are the two portions of the EW nucleus

And the structures supplied

A

Rostral

Caudal

Rostral-> constrictor pupillae

Caudal-> ciliaris

65
Q

Which part of the EW is stimulated by the pretectal nucleus?

A

Rostral

66
Q

Which nucleus stimulates the caudal portion of EW and what pathway is it involved in?

A

Accommodation/Near response

67
Q

Argyll-Robertson Pupil

ARP

A

Accommodation reflex preserved

Light reflex lost

Accommodates but does not react

68
Q

Causes of Argyll-Robertson Pupil

A

Neurosyphilis

DM

SLE

69
Q

Holmes Adie’s pupil

A

Sluggish pupillary constriction

Does not constrict

70
Q

Which type of receptor cells are found in the fovea centralis?

A

Cone cells which are responsible for colour vision

71
Q

Cortical arrangement of projections from visual field

A

Inverted and reversed from right to left

72
Q

Blood supply of optic nerve

A

Ophthalmic artery

73
Q

Blood supply of optic chiasm

A

Superior:

Small perforators from ACA/AComm

Inferior:

Posterior circulation

Superior hypophyseal artery (ICA)

The central portion is exclusively supplied by the inferior netwok

74
Q

Blood supply of optic tract

A

Anterior choroidal

75
Q

Blood supply of LGN

A

Anterior and posterior choroidal arteries

76
Q

Draw the light reflex

A
77
Q

What are the components of the convergence reflex

A

Pupillary constriction

Ocular convergence

Thickening of lengs to accommodate near vision

78
Q

Afferent limb of accommodation rfelx

A

Afferents to primary visual cortex

79
Q

Efferent limb of accommodation reflex

A

Impulses originating in the visual association cortex, traversing the superior brachium and terminating in the pretectal area and superior colliculus

Superior colliculus stimulates CN3 MR portion and EW nucleus

80
Q

Manifestation of optic nerve lesions

A

Complete- monocoular blindness

Partial- result in scotoma with central and then peripheral.

81
Q

Why does an incomplete lesion of optic nerve result in scotoma

A

The papillomacular bundle conveying central vision is very vulnerable to extrinsic compression

Usually spreads from central to peripheral part of visual field rather than the other way round

82
Q

Lesion location

A

Incomplete unilateral CN 2 lesion

83
Q

Lesion location

A

Unilatearl complete prechiasmatic CN II lesion

84
Q

def: Scotoma

A

Darkness

85
Q

Possible manifestations of junctional lesions

A

Possible field defects:

Junctional scotoma of Traquair:

Monocular temporal field defect (pressure on crossing nasal fibres)

Monocular nasal field defect (pressure on crossing temporal fibres)

Junctional scotoma:

Monocular scotoma (pressure on optic nerve), contralateral superior temporal field defect (involvement of crossing nasal fibres)

86
Q

Lesion location

Monocular temporal field defect

A

Junctional lesion

(Junctional scotoma of Traquair)

87
Q

Lesion location

Monocular nasal field defect

A

Junctional lateral lesion

Junctional scotoma of Traquair

88
Q

Ipsilateral scotoma

Contralateral superior temporal field defect

A

Junctional scotoma

89
Q

Lesion location

A

Junctional lesion

90
Q

Anatomical basis of junctional scotoma

A

Lesions at the junction between the optic nerve and chiasm may damage both optic nerve fibres and fibres of Willebrand’s knee (which are from inferonasal quadranat of optic nerve-> superior temporal field defect)

Ipsilateral compresison on optic nerve results in central scotoma

91
Q

Willebrand’s Knee

A

Thought to be a loop of decussating fires that detours into contralateral optic nerve before entering optic tract

Carries inferior nasal quadrant fibres so damage results in contralateral superior temporal hemianopia

92
Q

Is Willebrand’s knee real?

A

Horton 1997 Trans Am Ophthal soc

Study in monkeys and humans involving injection of radioactive dye

Did not find decussating fibres detouring into ocontralateral optic nerve.

After monocular enucleation found that fibres were drawn into the entry zone of degenerating optic nerve

Not due to decussation but rather due to compression of optic chiasm and nerve atrophy

93
Q

Anterior chiasmal syndrome

A

Junctional scotoma

Junctoinal scotoma of Traquair

94
Q

Middle chiasmal lesion

A

Bitemporal hemianopia

95
Q

Posterior chiasmal lesions

A

Smaller paracentral bitemporal field loss as macular fibres cross more posteriorly in the chiasm

Posterior lesions may also involve the optic tract and cause contralateral homonymous hemianopia.

96
Q

Prefixed chiasm

A

Overlying the tuberculum sellae

97
Q

Post-fixed chiasm

A

Overlying the dorsum sellae

98
Q

Optic tract lesions

A

Incongruous homonymous hemianopia

99
Q

What is the rule of congruity?

A

The more posterior the lesion in the retrogeniculate visual pathway, the more congruous the visual field defect

100
Q

Why does the rule of congruity not apply to homonymous hemianopias?

A

As homonymous hemianopias are nonlocalising

101
Q

Homonymous hemianopia localises to which portion of the visual field?

A

Retrochiasmal

102
Q

A patient is having an anterior temporal lobectomy for the treatment of seizures. What is the anterior extent of Meyer’s loop in the temporal lobe?

A

A quantitative analysis of visual field defects related to anterior temporal lobectomy estimated an anterior extent of Meyer’s loop of 2.5 cm and a posterior extent of 7.5 cm with macular involvement at a resection length of 5.8 cm. Therefore, an anterior temporal lobectomy may produce some degree of a homonymous visual field defect when the resection is greater than 2.5 cm and a complete homonymous visual field defect when the resection is greater than 8 cm.

103
Q

Which of the following may be seen with a homonymous hemianopia associated with a parietal lobe lesion?

Relative afferent pupillary defect

Macular sparing

Impairment of smooth pursuit towards the side of the lesion

Ipsilateral sensory changes

A

Impairment of smooth pursuit towards the side of the lesion

104
Q

A right-handed patient is unable to read his own handwritten words. He also has a right homonymous visual field defect due to a stroke in the territory of the left posterior cerebral artery affecting the left occipital lobe. Which other structure is affected by the stroke?

Right angular gyrus

Splenium of the corpus callosum

Optic chiasm

Midbrain

A

Splenium of the corpus callosum

This patient has alexia without agraphia, which is a disconnection syndrome between the dominant angular gyrus (region of language processing in anterolateral parietal lobe) and the occipital lobe. Visual information is received by the right occipital lobe and is normally transferred to the left angular gyrus by the corpus callosum. This cannot occur if the splenium of the corpus callosum is damaged as in this case. The patient can write because the structures anterior to the splenium of the corpus callosum are intact, but cannot read these words.

105
Q

What is the natural history of homonymous hemianopias?

Do not improve

Improve usually within the first 3 months and not after 6 months

Continuous improvement throughout life

Improvement up to 2 years after onset

A

A large natural history study of 263 homonymous hemianopias of various etiologies found that almost 40% improved. Improvement decreased with increasing time after injury. In most cases, improvement was within the first 3 months after injury and improvement after 6 months was mainly due to improvement in the patient’s ability to perform visual field testing reliably.

106
Q

A patient presents with left hemianesthesia and hemiparesis and the following visual field defect. Where is the most likely location of the lesion?

Bilateral optic nerves

Optic chasm

Lateral geniculate nucleus

Occipital lobe

A

Lateral geniculate nucleus

Compressive and infiltrative lesions of the lateral geniculate nucleus (LGN) may cause an incongruous homonymous hemianopia. Vascular lesions may cause a “sectoranopia” due to the distinctive blood supply and retinotopic organization of the LGN (shown below). When sectoranopias occur, they are usually very congruous due to the well-defined vascular territories of the LGN. Involvement of neighbouring structures in the thalamus and pyramidal tracts may result in contralateral hemianesthesia or hemiparesis.

107
Q
A

Homonymous horizontal sectoranopia

Posterior choroidal artery occ

108
Q
A

Sector sparing homonymous hemianopia

Anterior choroidal artery occlusion

109
Q

Meyer’s loop injury results in

A

Contralateral superior quadrantopia

110
Q

Complete colour blindness in presence of normal visual acuity suggests

A

Bilateral lesion in the inferiomedial temporooccipital lesion

111
Q
A

Macular sparing inferior quadranopsia

Upper bank of calcarine sulcus

112
Q
A

Macular sparing superior quadrantanopsia

Inferior bank of calcarine sulcus

113
Q
A

Macular sparing homonymous hemianopia

Both banks of calacrine cortex sparing occipital pole

114
Q

Incongruous hemianopia with RAPD

A

Pregeniculate retrochiasmal

115
Q

Microsurgical anatomy of the sagittal stratum

Di Carlo et al

Acta Neurochirugica

A
116
Q

What is this structure

A

Central retinal artery

117
Q

In which direction should the superior ophthalmic vein be retracted when accessing the orbital apex?

A

Laterally, if retracted medially it can restrict access to the apex

118
Q

https://www.neuroophthalmology.ca/textbook/disorders-of-eye-movements/v-prenuclear-disorders-brainstem/ii-internuclear-ophthalmoplegia-ino

A

NSx Neuroanatomy (25 decks)

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